Experimental autoimmune myasthenia gravis (EAMG) produced in C57B1/6 mice by immunization with Torpedo acetylcholine receptor has been modulated and attenuated by the in vivo administration of suppressor T cell lines and clones derived from lymph node cells from immunized animals. The mechanism of this suppression is being investigated with respect to its relationship to anti-idiotypic immunity and also with respect to the production of suppressor factors. The identity of the suppressor cells will be characterized by their surface markers, including idiotypic markers and intracellular enzyme containing organelles. Their in vitro action will be determined upon proliferation of sensitized cells to antigen and their effect upon secondary anti-acetylcholine receptor antibody production in vitro. The injection of these cells in vivo will be followed by their biologic influence on the course of development of EAMG as well as their distribution and homing in the recipient animal, their survival with an without the presence of interleukin II. The duration and specificity of their action in the recipient animal will be assessed and evidence for or against the development of a second wave of T cells bearing anti-idiotypic receptors investigated. These lines will be characterized by their surface markers, ability to "help" B cells produce anti-AChR antibody in vitro and in vivo, and to produce delayed type hypersensitivity reactions in vivo. We will determine if disease can be produced by means of cell transfers with helper lines in the absence of antigen and whether disease produced by AChR immunization can be blocked by prior treatment with attenuated cell lines.